Abstract
Inflammation of the skin is the pathological base of contact dermatitis (CD), and cytokines are very important in its pathogenesis. Recently it has been shown that interferon (IFN)-γ, and the IFN-γ dependent chemokines, monokine induced by IFN-γ (MIG), IFN-γ-induced protein 10 (IP-10), and IFN-inducible T cell alpha chemoattractant (I-TAC), play an important role in CD.
Allergic CD (ACD) is a T-cell-mediated disease in which expression of a distinct repertoire of chemokines results in the recruitment of effector T cells into the skin.
An increased expression of MIG, IP-10 and I-TAC in the skin has been observed by many studies in ACD, but not in irritant CD. The IFN-γ dependent chemokines are produced by keratinocytes, mainly during the clinically inflammatory phase of ACD.
Also chemokine (C-X-C motif) receptor (CXCR) 3, the common receptor of the three IFN-γ dependent chemokines, is upregulated in chemical-induced allergic skin responses when compared with irritant skin responses. However, other studies have shown a low level increase of IP-10 in irritant sodium dodecyl sulphate dermatitis.
The above mentioned results show that although skin inflammation contact sensitizer-induced is similar to irritant-induced, the regulation of allergic inflammation-related gene MIG and IP-10, could help to discriminate skin sensitization from chemically irritation
